Abstract

In vivo longitudinal (T1) and transverse (T2) relaxation times of hepatic intracellular and extracellular sodium were studied in rats with sham burn or burn injury with 23Na NMR spectroscopy and shift reagent. Burn injury decreases hepatic extracellular sodium content by 17% compared with sham burn, whereas it increases the percent of the fast T2 component of extracellular sodium, suggesting an increase in the fraction of bound Na+/- sites in the extracellular space. It is interesting that the relaxation characteristics of intracellular sodium remained unchanged despite a 57% increase in intracellular sodium content, suggesting the increase in intracellular free sodium is matched by either a proportional increase in intracellular bound sodium or an uncovering of ordered domain sites that can preferentially orient rapidly exchanging sodium ions. This study also demonstrated that spin lattice (T1) relaxation rates or the percent contribution of the fast/slow T2 components of the combined intracellular/extracellular 23Na signal (before the infusion of shift reagent) may also be sensitive to changes in intracellular sodium levels during pathologic changes.

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